Linked Life Data

15289328

Source:http://linkedlifedata.com/resource/pubmed/id/15289328

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
15
pubmed:dateCreated
2004-8-3
pubmed:abstractText
We previously showed, by immunohistochemistry with phospho-specific antibodies, increased phosphorylation (activation) of Akt (Ser(473)) [phosphorylated Akt (pAkt)] in high-Gleason grade prostate cancer (Malik SN, et al., Clin Cancer Res 2002;8:1168-71). Elevation of pAkt was accompanied by decreased phosphorylation of extracellular signal-regulated kinase (ERK) 1/2 (Thr(202)/Tyr(204)) [phosphorylated ERK (pERK)], indicative of inactivation. In this report, we determined whether increased pAkt and decreased pERK predicted clinical outcome. Prostate-specific antigen (PSA) failure (detectable and rising PSA) versus PSA non-failure (undetectable PSA 5 years after prostatectomy) was used as a surrogate for clinical outcome. Prostate tumors from cases of PSA failure versus non-failure were stained for pAkt and pERK. A significant increase in mean pAkt staining (P < 0.001) in the PSA failures versus non-failures was seen based on the Wilcoxon signed ranks test [222.18 +/- 33.9 (n = 37) versus 108.79 +/- 104.57 (n = 16)]. Using the best-fitting multiple logistic regression equation, a 100-point increase in pAkt staining resulted in a 160% increase in the odds of being a PSA failure. There was decreased staining for pERK in PSA failures versus non-failures: a 100-point decrease resulted in an 80% increase in the odds of being a PSA failure. Each of these effects assumed the other biomarker was held constant. The area under the receiver-operating characteristic curve for these two biomarkers predicting PSA failure was 0.84, indicating excellent discrimination between PSA failure and non-failure cases. These data indicate that increased pAkt, alone or together with decreased pERK, is an important predictor of probability of PSA failure. However, pERK alone was not a significant predictor of PSA failure.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
0008-5472
pubmed:author
pubmed:issnType
Print
pubmed:day
1
pubmed:volume
64
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
5232-6
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed-meshheading:15289328-Adult, pubmed-meshheading:15289328-Aged, pubmed-meshheading:15289328-Aged, 80 and over, pubmed-meshheading:15289328-Disease-Free Survival, pubmed-meshheading:15289328-Humans, pubmed-meshheading:15289328-Immunoenzyme Techniques, pubmed-meshheading:15289328-Male, pubmed-meshheading:15289328-Middle Aged, pubmed-meshheading:15289328-Mitogen-Activated Protein Kinase 1, pubmed-meshheading:15289328-Mitogen-Activated Protein Kinase 3, pubmed-meshheading:15289328-Mitogen-Activated Protein Kinases, pubmed-meshheading:15289328-Phosphorylation, pubmed-meshheading:15289328-Predictive Value of Tests, pubmed-meshheading:15289328-Prostate-Specific Antigen, pubmed-meshheading:15289328-Prostatectomy, pubmed-meshheading:15289328-Prostatic Neoplasms, pubmed-meshheading:15289328-Protein-Serine-Threonine Kinases, pubmed-meshheading:15289328-Proto-Oncogene Proteins, pubmed-meshheading:15289328-Proto-Oncogene Proteins c-akt
pubmed:year
2004
pubmed:articleTitle
Phosphorylation of Akt (Ser473) is an excellent predictor of poor clinical outcome in prostate cancer.
pubmed:affiliation
Department of Surgery, University of Texas Health Science Center at San Antonio, 7703 Floyd Curl Drive, San Antonio, TX 78229-3900, USA. kreisberg@uthscsa.edu
pubmed:publicationType
Journal Article